近日,来自天津医科大学肿瘤研究所的研究人员在Molecular Cancer杂志上发表了题为“The m6A demethylase ALKBH5-mediated upregulation of DDIT4-AS1 maintains pancreatic cancer stemness and suppresses chemosensitivity by activating the mTOR pathway”的文章,该研究揭示了ALKBH5介导的m6A修饰导致DDIT4-AS1在胰腺导管腺癌(PDAC)中过表达,DDIT-AS1通过破坏DDIT4的稳定性和激活mTOR通路而增加肿瘤的干性并抑制对GEM的化疗敏感性。靶向DDIT4-AS1及其通路可能是治疗PDAC化疗耐药的有效策略。
Yi Zhang et al. The m6A demethylase ALKBH5-mediated upregulation of DDIT4-AS1 maintains pancreatic cancer stemness and suppresses chemosensitivity by activating the mTOR pathway. Mol Cancer. 2022 Sep 2;21(1):174. doi: 10.1186/s12943-022-01647-0.